HIV coinfection was associated with a 3.7-fold increase in the risk of non-liver-related cancer among patients with hepatitis C virus infection, a new study found.
Patients with hepatitis C virus (HCV) infections who had an HIV coinfection had a 3.7-fold higher risk of non-liver-related cancer than those without HIV coinfection, according to a new study in France.
The study, published in HIV Medicine, included 548 patients coinfected with HCV and HIV and 2016 patients infected with HCV only. The participants were part of two multicenter, prospective, nationwide French cohort studies, and all were treated with direct-acting antivirals (DAA) and followed for up to three years.
“(I)n a population of HIV/HCV-coinfected participants with controlled HIV viral load, HIV coinfection was associated with a 3.7-fold higher risk of non-liver-related cancers at 3 years after DAA initiation, compared with HCV-monoinfected participants,” the authors wrote.
The study was led by Mathieu Chalouni, PhD, of the University of Bordeaux and supported by the French National Agency for Research on Aids and Viral Hepatitis. HIV/HCV-coinfected patients were from the ANRS CO13 HEPAVIH cohort, and HCV-monoinfected patients were from the ANRS CO22 HEPATHER cohort.
The primary outcome was time between the start of DAA treatment and occurence of non-liver-related cancer. The HIV/HCV coinfection group reported 22 cases of non-liver-related cancer, including non-melanoma skin, anal, lung, melanoma, nasopharynx, prostate, cervical and non-Hodgkin lymphoma. The group with HVC infection only reported 28 cases of non-liver-related cancer, including non-melanoma skin, pancreas, colon-rectal, lung, rengal-urethra and prostate.
The total effect of HIV coinfection was a 3.7-fold increase in risk of non-liver-related cancer (hazard ratio = 3.7, 95% Confidence Interval: 1.7–7.0) compared with HCV monoinfected patients. That increased risk was predominantly associated with a pure direct effect of HIV coinfection (HR = 3.4, 95% CI: 1.7–6.6). The total indirect effect, reflecting higher rates of alcohol consumption, tobacco consumption and metabolic syndrome among patients infected with HIV, was not significantly associated with increased risk of non-liver-associated cancer (HR = 1.1, 95% CI: 0.8–1.5).
“To our knowledge, no other study has evaluated the potential impact of HIV coinfection on the risk of non-liver-related cancers after DAA treatment in HCV-infected participants or the potential mediating effect of alcohol consumption, tobacco consumption and metabolic syndrome on the relationship between HIV coinfection and risk of non-liver-related cancers,” the authors wrote.
Among the coinfected group, 17 of 22 cancer occurrences were unrelated to oncogenic viruses, which HIV-coinfected patients are more exposed to. Even when excluding oncogenic virus-related cancers, HIV coinfection was associated with a 3.1-fold increase in risk of non-liver-related cancers (HR = 3.1, 95% CI: 1.6–4.9).
Limitations of the study include that it included participants from two different cohorts, which could have led to differences in classification. Also consumption of alcohol and tobacco was measured at baseline only, so investigators could not account for differences in past consumption or cessation.
Hepatitis C infection is primarily transmitted via injection-drug use, but sexual transmission is an important concern. According to the US Center for Disease Control and Infection, about 21% of adults with HIV also tested positive for HCV infection. Studies have shown that a majority of those with HIV/HCV coinfection were intravenous drug users, representing a population that is a high priority for treatment.
Work is ongoing to identify and address HIV/HCV coinfections. A study in San Diego examined the use of universal HIV and HCV screening in two emergency departments, finding that universal screening may identify cases among patients not likely to get tested and may reconnect patients with HIV who have fallen out of care.